The Problem. The positive psychology movement has led to an increased attention in organizational virtuousness, engagement, and happiness. Though attention has been devoted to studying the relationship between organizational virtuousness and performance, there is limited research that explores the relationship between employees' perception of organizational virtuousness and work engagement. The Solution. A cross-sectional survey was carried out on a sample of knowledge workers from diverse Indian industries. The findings of the study showed that the employees' perception of organizational virtuousness predicts work engagement not only directly but also indirectly through happiness. The Stakeholders. Managers can nurture organizational virtuousness in organizations to enhance employee happiness and promote a more engaged workforce. Considering the findings of the study, Human Resource Development (HRD) professionals should make the best use of their human capital by fostering positive psychological states such as work engagement.
Objective-African-American (AA) women with breast cancer are more likely to have advanced disease at diagnosis, higher risk of recurrence and poorer prognosis than Caucasian (CA) women. We have recently shown higher insulin-like growth factor II (IGF-II) expression in paired breast tissue samples from AA women as compared to CA women. IGF-II is a potent mitogen that induces cell proliferation and survival signals through activation of the IGF-I and Insulin receptors (IGF-IR, IR) while IGF-II circulating levels are regulated by cellular uptake through the IGF2 receptor. We hypothesize that differential expression of the IGFIR and IGF2R among AA and CA women potentiates IGF-II mitogenic effects, thus contributing to the health disparity observed between these ethnic groups.Design-We examined IGF-IR and IGF2R mRNA, protein expression and IGF1R phosphorylation in paired breast tissue samples from AA and CA women by Real Time-PCR, western blot analysis, immunohistochemistry and ELISA techniques.Results-Our results showed significantly increased expression of IGF1R in AA normal tissues as compared to CA normal tissues. IGF1R expression was similar between AA normal and malignant tissues, while IGF1R, IRS-1 and Shc phosphorylation was significantly higher in AA tumor samples. Significantly higher levels of IGF2R were found in CA tumor samples as compared to AA tumor samples.Conclusions-We conclude that IGFIR and IGF2R differential expression may contribute to the increased risk of malignant transformation in young AA women and to the more aggressive breast cancer phenotype observed among AA breast cancer patients and represent, along with IGF-II, potential therapeutic targets in breast cancer.
Objective Increased risk of cancer and other adult diseases have been associated with perinatal exposure to adverse conditions such as stress and famine. Recently, Insulin-like growth factor II (IGF-II) was identified as the first gene associated with altered expression caused by fetal exposure to poor nutrition. IGF-II regulates fetal development and breast cancer cell survival, in part, by regulating anti-apoptotic proteins through activation of the IGF-I and insulin receptors. African-American (AA) women have a lower overall breast cancer (BC) incidence, however, they present with advanced disease at diagnosis, poorer prognosis and lower survival than Caucasian (CA) women. The reasons for the BC survival disparity are not well understood. We hypothesize that IGF-II plays a role in the survival disparity observed among AA breast cancer patients by stimulating rapid tumor growth, inhibiting apoptosis and promoting metastasis. Design This study examines IGF-II expression and regulation of the anti-apoptotic proteins Bcl-2, Bcl-XL and survivin in Hs578t (ER−), CRL 2335 (ER−) and CRL 2329 (ER+) breast cancer cells and compares with the expression of these proteins in paired breast tissue samples from AA and CA women by qRT PCR and Western blotting. Results IGF-II expression was significantly higher in AA cell lines and tissue samples when compared to Caucasians. IGF-II siRNA treatment decreased antiapoptotic protein levels in all cell lines (regardless of ER status). These effects were blocked by the addition of recombinant IGF-II. Of significance, IGF-II expression and regulation of Bcl-XL and survivin in cell lines correlated with their expression in paired breast tissues. Conclusions IGF-II and the antiapoptotic proteins differential expression among AA and CA patients may contribute to the breast cancer survival disparities observed between these ethnic groups.
We showed that when IGF-II is highly expressed in breast tissues and cell lines the IGF-1 receptor signaling pathway is highly activated. Since IGF-II activates the insulin receptor (INSR), we propose that the INSR signaling is also activated in this system. We examined the expression of both INSR isoforms, INSR-A, INSR-B, and the downstream signaling pathways in breast cancer cells and in paired (normal/tumor) breast tissues from 100 patients. Analysis was performed by Real Time-PCR, Western blot, immunohistochemistry and Phospho-ELISA techniques. Tumor tissues and cell lines from African American patients (AA) expressed higher levels of INSR-A, but lower levels of INSR-B. In accordance, IRS-1 and FAK activation were significantly increased in these women. We conclude that higher INSR-A and lower INSR-B contributes to higher proliferation and lower metabolic response. Thus, differential expression of INSR isoforms represents a potential biological link between breast cancer and diabetes.
Insulin-like growth factor II (IGF-II) plays a pivotal role in fetal and cancer development by signaling through the IGF-I and insulin receptors and activating the estrogen signaling cascade. We previously showed that precursor IGF-II (proIGF-II, the predominant form expressed in cancer) and not mature IGF-II (mIGF-II) blocks resveratrol (RSV) (a phytoalexin/anticancer agent)-induced cell death in MCF-7 cells. We hypothesize that proIGF-II regulates antiapoptotic proteins and/or the mitochondria to inhibit RSV actions and promote cell survival. This study examines the effect of mIGF-II and proIGF-II on survivin expression and mitochondrial polarization in response to RSV. RSV inhibits survivin expression and stimulates mitochondrial depolarization, caspase 7 activation and cell death. These effects were completely blocked by the addition of proIGF-II. RSV treatment had no effect on transfected MCF-7 cells constitutively expressing proIGF-II, while IGF-II siRNA transfection decreased survivin levels. Our results provide new insights for the potential use of proIGF-II as target for new anticancer therapies.
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